NSAID's Flashcards
What are NSAID’s
-non-steroidal inflammatory drugs
Describe how pain sensation is felt ( eg right hand )
- Afferent nerve is stimulated by mediators of inflammation or physical damage
- nerve impulse taken to 2nd order neuron and goes to left spinothalamic track up stem and to thalamus
- synapse with 3rd order neuron which propagates to somatosensory cortex and that discerns which part is injured and pain perceived
How does pain aid in inflammation
-stimulated afferent nerves release Substance P and CGRP which enhance inflammation response
How do inflammation mediators cause pain
List the mediators and the receptors they bind to
/they bind to noiceptors on afferent nerve nearby depolarizing the neuron
- bradykirin B2
- prostaglandin : prostanoid receptors
How are mediators for inflammation made by the body
- damaged membrane releases phospholipase AC which converts phospholipid into arachadonic acid
- LPO converts the acid into leukotrines
- COX 1 and 2 convert it into prostaglandins , thromboxane and prostacyclin
Diff of Cycloxygenase 1 and 2
- secreted continuously and is for normal homeostasis
- secreted only during inflammation and is for inflammation response
What is the MOD of action of NSAID’s
-block COX enzymes and there will be no production of inflammation mediators ( prostaglandins )
3 types of nsaids and examples
1 Cox 1 selective : aspirin
2 non-selective : ibuprofen , paracetamol
3 Cox 2 selective : celecoxib
4 Aim or responses of nsaids
- anti inflammatory
- antipyretic : reduces fever
- analgesic : reliefs pain
- anti platelets : stop clotting of blood
What’s does Cox 1 do. It’s effects
/produces prostaglandins which have
- inflammation effect
- pain
- swelling
- aid in renal flow via constriction
- aid in secretion of gastric muscus
/converts arachadonic acid into thromboxane which aids in blood clotting
What does Cox 2 do. It’s effects
/ converts arachadonic acid into prostaglandins
- inflammation
- pain
- bronchodilaton
- swelling
- inhibits blood clot
What does LPO do and it’s effects
-converts arachadonic acid into leukotrines
1 increase respiratory tract mucus production
2 bronchospasm
3 inflammation response
Effects of inhibiting Cox 1
- blot does not clot ( excessive hemorrhage )
- gastric ulcers
- renal failure
- inflammation , pain , swelling and fever subside
Effects of inhibiting Cox 2
- blood easily clots ( stroke infarction )
- bronchospasm
What makes prostacyclin , it’s function and effects if deficient
- made by endothelial cells
- causes vasodilation to inhibit blood clot
-excessive blood clot ( stroke , infarction )
2 other drugs to never take with nsaids
- diuretics
- ACEI
How do nsaids aid in renal failure
-causes renal arteriole to dilate and important for glomerular filtration
How does Cox 2 cause rheumatoid arthritis
-it aids in inflammatory response due to immune cells attacking the bodies own joints
What’s the effect of aspirin irreversibly inhibiting Cox 1
-platelets are irreversibly inhibited and since they have no nucleus they can’t make more and will have to wait for turnover
What do leukotrines lead to and how to stop it
- it leads to asthma
- use leukotrine receptor antagonists to stop leukotrines from binding
Why suppress pain and fever with nsaids
- may produce shock , interfere with quality of life , may frighten the patient
- incapacitated people , inactivates metabolism of important processes
How do IL-1 , TNF-a and prostaglandins cause fever
What won’t nsaids reduce
-they cause the hypothalamus to release PGE’s which cause body temperature to increase
/normal temp or elevated temp of heat stroke
What is contraindicated and indications
/reasons to not take a specific drug due to the effects
-reasons to take a drug due to the benefits
Why not use aspirin in gout patients
-aspirin increases Uric acid conc in urine which may be crystallized and deposit in joints
